SLC35G1 (solute carrier family 35 member G1) is a 10-transmembrane-spanning transporter with multiple physiological roles. Functionally, SLC35G1 serves as the basolateral membrane transporter responsible for intestinal citrate absorption, mediating citrate release into the bloodstream following luminal uptake 1. The transporter exhibits extreme chloride sensitivity at physiologically relevant extracellular concentrations, representing the first identified basolateral intestinal transporter with such pronounced chloride dependence 1. At the cellular level, SLC35G1 associates with stromal interaction molecule 1 (STIM1) and modulates calcium homeostasis by reducing plasma membrane Ca²⁺-ATPase (PMCA) activity 2, consistent with a regulatory role in calcium efflux prevention. Pathologically, SLC35G1 has emerged as a novel autism spectrum disorder (ASD) candidate gene; mice with heterozygous Slc35g1 deletion exhibit defects in interactive social behaviors 3. Additionally, SLC35G1 expression changes in CD8 effector T cells correlate with Graves' ophthalmopathy disease phenotypes, potentially contributing to disease progression through fibrosis-related pathways 4. Genome-wide association studies identified SLC35G1 variants (rs146091982) as significant risk factors for cannabis dependence severity, with functions related to neuronal calcium homeostasis 5. Together, these findings suggest SLC35G1's involvement extends from nutrient absorption to neuropsychiatric and immune-mediated disease pathogenesis.